scholarly journals Naja atra Cardiotoxin 1 Induces the FasL/Fas Death Pathway in Human Leukemia Cells

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2073
Author(s):  
Jing-Ting Chiou ◽  
Liang-Jun Wang ◽  
Yuan-Chin Lee ◽  
Long-Sen Chang
Keyword(s):  
P38 Mapk ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Human Leukemia ◽  
U937 Cells ◽  
Fasl Expression ◽  
Mechanistic Pathway ◽  
Leukemia Cell Lines ◽  
Sirna Knockdown ◽  
Naja Atra

This study aimed to investigate the mechanistic pathway of Naja atra (Taiwan cobra) cardiotoxin 1 (CTX1)–induced death of leukemia cell lines U937 and HL-60. CTX1 increased cytoplasmic Ca2+ and reactive oxygen species (ROS) production, leading to the death of U937 cells. It was found that Ca2+-induced NOX4 upregulation promoted ROS-mediated p38 MAPK phosphorylation, which consequently induced c-Jun and ATF-2 phosphorylation. Using siRNA knockdown, activated c-Jun and ATF-2 were demonstrated to regulate the expression of Fas and FasL, respectively. Suppression of Ca2+-mediated NOX4 expression or ROS-mediated p38 MAPK activation increased the survival of U937 cells exposed to CTX1. FADD depletion abolished CTX1-induced cell death, caspase-8 activation, and t-Bid production, supporting the correlation between the Fas death pathway and CTX1-mediated cytotoxicity. Among the tested N. atra CTX isotoxins, only CTX1 induced Fas and FasL expression. Chemical modification studies revealed that intact Met residues were essential for the activity of CTX1 to upregulate Fas and FasL expression. Taken together, the data in this study indicate that CTX1 induces c-Jun-mediated Fas and ATF-2-mediated FasL transcription by the Ca2+/NOX4/ROS/p38 MAPK axis, thereby activating the Fas death pathway in U937 cells. Furthermore, CTX1 activates Fas/FasL death signaling in the leukemia cell line HL-60.

scholarly journals Regulation of platelet-derived growth factor gene expression by transforming growth factor beta and phorbol ester in human leukemia cell lines.

1987 ◽  
Vol 7 (10) ◽  
pp. 3656-3662 ◽  
Author(s):  
T P Mäkelä ◽  
R Alitalo ◽  
Y Paulsson ◽  
B Westermark ◽  
C H Heldin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Line ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Human Leukemia ◽  
U937 Cells ◽  
Tgf Beta ◽  
Leukemia Cell Lines

We studied the expression of the genes encoding the A and B chains of platelet-derived growth factor (PDGF) in a number of human leukemia cell lines. Steady-state expression of the A-chain RNA was seen only in the promonocytic leukemia cell line U937 and in the T-cell leukemia cell line MOLT-4. It has previously been reported that both PDGF A and PDGF B genes are induced during megakaryoblastic differentiation of the K562 erythroleukemia cells and transiently during monocytic differentiation of the promyelocytic leukemia cell line HL-60 and U937 cells. In this study we show that PDGF A RNA expression was induced in HL-60 and Jurkat T-cell leukemia cells and increased in U937 and MOLT-4 cells after a 1- to 2-h stimulation with an 8 pM concentration of transforming growth factor beta (TGF-beta). PDGF A RNA remained at a constant, elevated level for at least 24 h in U937 cells, but returned to undetectable levels within 12 h in HL-60 cells. No PDGF A expression was induced by TGF-beta in K562 cells or in lung carcinoma cells (A549). Interestingly, essentially no PDGF B-chain (c-sis proto-oncogene) RNA was expressed simultaneously with PDGF A. In the presence of TGF-beta and protein synthesis inhibitors, PDGF A RNA was superinduced at least 20-fold in the U937 and HL-60 cells. PDGF A expression was accompanied by secretion of immunoprecipitable PDGF to the culture medium of HL-60 and U937 cells. The phorbol ester tumor promoter tetradecanoyl phorbol acetate also increased PDGF A expression with similar kinetics, but with a mechanism distinct from that of TGF-beta. These results suggest a role for TGF-beta in the differential regulation of expression of the PDGF genes.

Regulation of platelet-derived growth factor gene expression by transforming growth factor beta and phorbol ester in human leukemia cell lines

1987 ◽  
Vol 7 (10) ◽  
pp. 3656-3662
Author(s):  
T P Mäkelä ◽  
R Alitalo ◽  
Y Paulsson ◽  
B Westermark ◽  
C H Heldin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Line ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Human Leukemia ◽  
U937 Cells ◽  
Tgf Beta ◽  
Leukemia Cell Lines

We studied the expression of the genes encoding the A and B chains of platelet-derived growth factor (PDGF) in a number of human leukemia cell lines. Steady-state expression of the A-chain RNA was seen only in the promonocytic leukemia cell line U937 and in the T-cell leukemia cell line MOLT-4. It has previously been reported that both PDGF A and PDGF B genes are induced during megakaryoblastic differentiation of the K562 erythroleukemia cells and transiently during monocytic differentiation of the promyelocytic leukemia cell line HL-60 and U937 cells. In this study we show that PDGF A RNA expression was induced in HL-60 and Jurkat T-cell leukemia cells and increased in U937 and MOLT-4 cells after a 1- to 2-h stimulation with an 8 pM concentration of transforming growth factor beta (TGF-beta). PDGF A RNA remained at a constant, elevated level for at least 24 h in U937 cells, but returned to undetectable levels within 12 h in HL-60 cells. No PDGF A expression was induced by TGF-beta in K562 cells or in lung carcinoma cells (A549). Interestingly, essentially no PDGF B-chain (c-sis proto-oncogene) RNA was expressed simultaneously with PDGF A. In the presence of TGF-beta and protein synthesis inhibitors, PDGF A RNA was superinduced at least 20-fold in the U937 and HL-60 cells. PDGF A expression was accompanied by secretion of immunoprecipitable PDGF to the culture medium of HL-60 and U937 cells. The phorbol ester tumor promoter tetradecanoyl phorbol acetate also increased PDGF A expression with similar kinetics, but with a mechanism distinct from that of TGF-beta. These results suggest a role for TGF-beta in the differential regulation of expression of the PDGF genes.

scholarly journals 1-Phenyl-8-[[4-(pyrrolo[1,2-a]quinoxalin-4-yl)phenyl]methyl]-1,3,8-triazaspiro[4.5]decan-4-one: Synthesis, Crystal Structure and Anti-Leukemic Activity

Molbank ◽  
10.3390/m1113 ◽  
2020 ◽  
Vol 2020 (1) ◽  
pp. M1113
Author(s):  
Jean Guillon ◽  
Solène Savrimoutou ◽  
Sandra Rubio ◽  
Stéphane Moreau ◽  
Noël Pinaud ◽  
...  
Keyword(s):  
Leukemia Cell ◽  
Structure Characterization ◽  
Human Leukemia ◽  
U937 Cells ◽  
Quinoxaline Derivative ◽  
Cytotoxic Potential ◽  
X Ray ◽  
Leukemia Cell Lines ◽  
Ft Ir

1-Phenyl-8-[[4-(pyrrolo[1,2-a]quinoxalin-4-yl)phenyl]methyl]-1,3,8-triazaspiro[4.5]decan-4-one has been successfully synthesized via a multi-step pathway starting from 2-nitroaniline. Structure characterization of this original pyrrolo[1,2-a]quinoxaline derivative was achieved by FT-IR, 1H-NMR, 13C-NMR, X-Ray and HRMS spectral analysis. This title compound shows interesting cytotoxic potential against several human leukemia cell lines (K562, HL60, and U937 cells).

Ectopic Expression of CXCR5/BLR1 Accelerates Retinoic Acid- and Vitamin D3-Induced Monocytic Differentiation of U937 Cells

2002 ◽  
Vol 227 (9) ◽  
pp. 753-762 ◽  
Author(s):  
Traci E. Battle ◽  
Andrew Yen
Keyword(s):  
Retinoic Acid ◽  
Cell Differentiation ◽  
Ectopic Expression ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Human Leukemia ◽  
U937 Cells ◽  
Monocytic Differentiation ◽  
Dihydroxyvitamin D ◽  
Moderate Growth

The product of the blr1 gene is a CXC chemokine receptor (CXCR5) that regulates B lymphocyte migration and has been implicated in myelomonocytic differentiation. The U937 human leukemia cell line was used to study the role of blr1 in retinoic acid-regulated monocytic leukemia cell growth and differentiation. blr1 mRNA expression was induced within 12 hr by retinoic acid in U937 cells. To determine whether the early induction of blr1 might regulate inducible monocytic cell differentiation, U937 cells were stably transfected with blr1 (U937/blr1 cells). Ectopic expression of blr1 caused no significant cell cycle or differentiation changes, but caused the U937/blr1 cells to differentiate faster when treated with either retinoic acid or 1α,5-dihydroxyvitamin D3. Treated with retinoic acid, U937/blr1 cells showed a greater increase in the percentage of CD11b expressing cells than vector control cells. Retinoic acid also Induced a higher percentage of functionally differentiated blr1 transfectants as assessed by nitroblue tetrazolium reduction. U937/blr1 cells underwent moderate growth inhibition on treatment with retinoic acid. Similar results occurred with 1α,25-dihydroxyvitamin D3. Because blr1 was induced early during cell differentiation and because its overexpression accelerated monocytic differentiation, it may be Important for signals controlling cell differentiation.

Effects of carboplatin in combination with other anticancer agents on human leukemia cell lines

1993 ◽  
Vol 17 (2) ◽  
pp. 113-119 ◽  
Author(s):  
Yasuhiko Kano ◽  
Miyuki Akutsu ◽  
Kenichi Suzuki ◽  
Minoru Yoshida
Keyword(s):  
Cell Lines ◽  
Anticancer Agents ◽  
Leukemia Cell ◽  
Human Leukemia ◽  
Human Leukemia Cell ◽  
Leukemia Cell Lines

scholarly journals 2-Chloro-2′-deoxyadenosine induces apoptosis through the Fas/Fas ligand pathway in human leukemia cell line MOLT-4

Leukemia ◽  
2000 ◽  
Vol 14 (2) ◽  
pp. 299-306 ◽  
Author(s):  
Y Nomura ◽  
O Inanami ◽  
K Takahashi ◽  
A Matsuda ◽  
M Kuwabara
Keyword(s):  
Cell Line ◽  
Fas Ligand ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Human Leukemia ◽  
Human Leukemia Cell ◽  
Human Leukemia Cell Line
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